Vestibular migraine: clinical aspects and pathophysiology.

Department of Otolaryngology, University of Pittsburgh, Pittsburgh, PA 15213, USA. Electronic address: .
The Lancet Neurology (Impact Factor: 21.82). 07/2013; 12(7):706-15. DOI: 10.1016/S1474-4422(13)70107-8
Source: PubMed

ABSTRACT Vestibular migraine is becoming recognised as a distinct clinical entity that accounts for a high proportion of patients with vestibular symptoms. A temporal overlap between vestibular symptoms, such as vertigo and head-movement intolerance, and migraine symptoms, such as headache, photophobia, and phonophobia, is a requisite diagnostic criterion. Physical examination and laboratory testing are usually normal in vestibular migraine but can be used to rule out other vestibular disorders with overlapping symptoms. The pathophysiology of vestibular migraine is incompletely understood but plausibly could include neuroanatomical pathways to and from central vestibular structures and neurochemical modulation via the locus coeruleus and raphe nuclei. In the absence of controlled trials, treatment options for patients with vestibular migraine largely mirror those for migraine headache.

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    ABSTRACT: Vestibular migraine (VM) is a common disorder in which genetic, epigenetic, and environmental factors probably contribute to its development. The pathophysiology of VM is unknown; nevertheless in the last few years, several studies are contributing to understand the neurophysiological pathways involved in VM. The current hypotheses are mostly based on the knowledge of migraine itself. The evidence of trigeminal innervation of the labyrinth vessels and the localization of vasoactive neuropeptides in the perivascular afferent terminals of these trigeminal fibers support the involvement of the trigemino-vascular system. The neurogenic inflammation triggered by activation of the trigeminal-vestibulocochlear reflex, with the subsequent inner ear plasma protein extravasation and the release of inflammatory mediators, can contribute to a sustained activation and sensitization of the trigeminal primary afferent neurons explaining VM symptoms. The reciprocal connections between brainstem vestibular nuclei and the structures that modulate trigeminal nociceptive inputs (rostral ventromedial medulla, ventrolateral periaqueductal gray, locus coeruleus, and nucleus raphe magnus) are critical to understand the pathophysiology of VM. Although cortical spreading depression can affect cortical areas involved in processing vestibular information, functional neuroimaging techniques suggest a dysmodulation in the multimodal sensory integration and processing of vestibular and nociceptive information, resulting from a vestibulo-thalamo-cortical dysfunction, as the pathogenic mechanism underlying VM. The elevated prevalence of VM suggests that multiple functional variants may confer a genetic susceptibility leading to a dysregulation of excitatory-inhibitory balance in brain structures involved in the processing of sensory information, vestibular inputs, and pain. The interactions among several functional and structural neural networks could explain the pathogenic mechanisms of VM.
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    ABSTRACT: Persons with vestibular disorders experience symptoms of dizziness and balance dysfunction, resulting in falls, as well as impairments of daily life. Various interventions provided by physical therapists have been shown to decrease dizziness and improve postural control. In the present review, we will focus on the role of physical therapy in the management of vestibular symptoms in patients with peripheral and central vestibular disorders. Persons with both acute and chronic central and peripheral vestibular disorders improve with vestibular rehabilitation. New interventions during the past 5 years have been designed to enhance recovery from problems with balance and dizziness. Examples include the use of virtual reality, vibrotactile feedback, optokinetic flow, YouTube videos, and innovative methods to change the gain of the vestibulo-ocular reflex (VOR). Patients with central and peripheral vestibular disorders benefit from physical therapy interventions. Advances in physical therapy interventions include new methods to stimulate adaptation of the VOR and the vestibulospinal systems.
    Current Opinion in Neurology 12/2014; · 5.73 Impact Factor
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    ABSTRACT: Vestibular migraine (VM), a common cause of vestibular symptoms within the general pop-ulation, is a disabling and poorly understood form of dizziness. We sought to examine the underlying pathophysiology of VM with three studies, which involved the central synthesis of canal and otolith cues, and present preliminary results from each of these studies: (1) VM patients appear to have reduced motion perception thresholds when canal and otolith signals are modulated in a co-planar manner during roll tilt; (2) percepts of roll tilt appear to develop more slowly in VM patients than in control groups during a centrifugation par-adigm that presents conflicting, orthogonal canal and otolith cues; and (3) eye movement responses appear to be different in VM patients when studied with a post-rotational tilt paradigm, which also presents a canal–otolith conflict, as the shift of the eye's rotational axis was larger in VM and the relationship between the axis shift and tilt suppression of the vestibulo-ocular reflex differed in VM patients relative to control groups. Based on these preliminary perceptual and eye movement results obtained with three different motion paradigms, we present a hypothesis that the integration of canal and otolith signals by the brain is abnormal in VM and that this abnormality could be cerebellar in origin. We provide potential mechanisms that could underlie these observations, and speculate that one of more of these mechanisms contributes to the vestibular symptoms and motion intolerance that are characteristic of the VM syndrome.
    Frontiers in Neurology 11/2014; 5:233.


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Jun 2, 2014